Would a prestigious national institution invite a Holocaust denier to speak about World World II, or a member of the KKK to speak about race relations?

We can't know what they were thinking when the NIH extended their invitation to Dr. Shorter, who is certainly no expert on any aspect of ME/CFS. But we do know that inviting a man who is so outspoken in his absolute denial of the disease reflects very poorly on the attitudes of the institution that recently pledged to take ME/CFS "very seriously."

You can read more about Dr. Shorter's invitation as well as his disparagement of ME/CFS patients HERE.

Dr. Shorter is scheduled to speak on November 9. Please send a letter to your representative today.______________________________From Solve ME/CFS Initiative

BREAKING NEWS: Last week, deeply troubling information was discovered on an archived National Institutes of Health (NIH) webpage. A lecture titled “Chronic Fatigue Syndrome in Historical Perspective” is scheduled for Wednesday, November 9, to be presented by the controversial and inflammatory history professor Edward Shorter, PhD.

A professor of psychiatry and history at the University of Toronto, Shorter is an outspoken skeptic about the biological nature of ME/CFS. He has referred to the disease as both a “psychodrama” and a “psychic epidemic” and called the findings of the Institute of Medicine’s report on ME/CFS last year “junk science.”

Please note that this action is for REPRESENTATIVES ONLY, NOT SENATORS.

Please call the Washington DC office, not the district office, and ask to speak to the legislative assistant for health. If the legislative assistant is not available, you can ask to leave a message or immediately ask for the e-mail address of the legislative assistant to send him or her your request in writing.

Feel free to tell the legislative assistant your story, but remember to be very brief. Use the sample script below as a guide.

My name is _________. I’m a constituent in {city}. I am calling with an urgent request for Representative {NAME} to contact the National Institutes of Health. The NIH has invited an inflammatory and controversial speaker, Dr. Shorter, who denies that ME/CFS is a physical disease. Between 1 to 2.5 million Americans like me [or my family member] who are afflicted with the horrific, disabling, and costly disease myalgic encephalomyelitis, also known as chronic fatigue syndrome or ME/CFS. ME/CFS has no known cause, cure, diagnostic test, or FDA-approved treatment, and it often leaves patients bedridden for decades. Please urge Representative {NAME} to support patients and voice their concern about this troubling speaker who calls me [or my family member] “delusional.” May I have your e-mail address to send you additional information?

If you do not receive an e-mail address for a particular staffer, ask for the general comment e-mail address.Step 2: E-mail your representativeAfter you speak to the staff person by phone, it is always helpful to follow up with an e-mail. Download a helpful ME/CFS issue fact sheet here (http://solvecfs.org/wp-content/uploads/2016/11/SMCI-NIH-Response-Flaws-Flier.pdf) to include with your e-mail. Feel free to personalize the e-mail below.

Dear Congress Member [LAST NAME],

As a constituent and as a (caregiver to / loved one of) a patient with myalgic encephalomyelitis (ME), commonly known as chronic fatigue syndrome (CFS), I am bringing your attention to the immediate need for Congress to assist ME/CFS patients. In September, 55 bipartisan members of the House of Representatives joined together to write to NIH Director Francis Collins regarding ME/CFS. That letter was not enough, and we need your help now.As you may know, ME/CFS is a complex disease with no known cause, treatment, diagnostic tool, nor cure. The CDC estimates that up to 2.5 million Americans suffer from ME/CFS, and patients have lower quality of life scores than those with lung cancer, stroke, and rheumatoid arthritis. According to the 2015 Institute of Medicine Report on ME/CFS, the disease costs the U.S. economy an estimated $17-$24 billion per year.

And the NIH continues to disregard the legitimate needs of ME/CFS patients. On Wednesday, November 9, the NIH’s clinical center is scheduled to host a lecture given by Dr. Edward Shorter, a historian at the University of Toronto and one of the most controversial and inflammatory figures to the ME/CFS patient community. This man, despite overwhelming scientific evidence, does not believe ME/CFS is an actual disease—instead calling it a “psychic epidemic” perpetrated by “moaning and groaning victims” who are “delusional.” Dr. Shorter has written pieces so disparaging of patients that they were removed from circulation by Psychology Today.

The NIH is clearly not prioritizing a solution to ME/CFS when they provide a forum for a speaker who demeans patients and denies scientific findings. I am asking you to please stand with patients who are very ill with this very REAL physiological disease, as verified by thousands of published scientific articles.​Please contact NIH Director Francis Collins and ask him to

Present scientifically grounded information to NIH researchers. If the NIH insists on including an inflammatory and controversial speaker who offers no scientific rigor, please balance this with an opposing expert such as Mary Dimmock, author of 30 Years of Disdain: How HHS and a Group of Psychiatrists Buried Myalgic Encephalomyelitis.

Reaffirm the findings of the Institute of Medicine report that ME/CFS is a true physiological disease, not a psychological one.

Prioritize ME/CFS funding with substantial investment commensurate with the burden of this devastating disease.

Only continued oversight from you and your colleagues in Congress will induce the NIH to take the actions necessary to help patients.

Very truly yours,

(NAME)

Step 3: Let us know how it wentE-mail our advocacy and engagement manager, Emily Taylor (etaylor@solvecfs.org), to let us know your member of Congress received the message.

Thank you for doing your part to advocate on behalf of all the patients who suffer with this disease.

The IACFS/ME (International Association for CFS and ME) Conference is held every other year. This year it was held on October 27-30, at the Westin Fort Lauderdale Beach Resort in Fort Lauderdale, Florida.

This conference is a huge event, attracting researchers and clinicians from all over the world. There are workshops, presentations, poster sessions and numerous networking events. It is an exciting gathering, and a wonderful opportunity to hear the latest in ME/CFS research.

Traditionally, Dr. Komaroff gives a summary of the notable research presented at the conference. ​Mary Schweitzer has generously provided the summary below with this note: This is my best effort of transcribing Komaroff’s summary of the 2016 meeting - feel free to repost.

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Komaroff summary of 2016 IACFS/ME meeting

In the past two years, since the 2014 SF meeting the report of the IOM based on a review of other 9.000 published articles concludes that ME/CFS is a “biologically-based illness”

Announcement of expanded research activities by the National Institutes of Health and educational efforts by the Centers for Disease Control and Prevention.

Detailed analysis of the components of “post-exertional malaise” (Stanford)- Physical and cognitive exertion trigger PEM more often than emotional distress.- PEM includes not only fatigue, but also cognitive difficulties, sleep disturbances, headaches, muscle pain and flu-like symptoms- PEM lasts 3 or more days in approximately 25% of people.

Exercise testing in patients with ME?CFS vs. healthy controls:- Triggers a characteristic gene expression “signature” involving 15 cytokines/adipokines/growth factors (Stanford)- When repeated 24 hours after a first exercise test leads to a significant decline in peak heart rate (“chronotropic incompetence”), which could contribute to post-exertional malaise (U of the Pacific)- Leads to postural tachycardia after exercise (as contrasted to after tilt table testing) in a subset of ME/CFS patients and Gulf War Illness patients, due to increased sympathetic activity (Georgetown)

Exercise testing in patients with ME/CFS vs. healthy control subjects:- Leads to lower oxygen consumption and earlier conversion to anaerobic metabolism (Nova and Wisconsin)- Blood lactate levels in 2nd exercise test after 24 hours- ME/CFS patients lactate levels are higher at all work loads- Healthy controls: lactate leels are lower at all work loads.

Immunology:

Huge study: 192 cases, 392 healthy controls.- Levels of 17/51 cytokines/adipokines/growth factors were significantly different in ME/CFS than healthy controls- Most of the cytokines were pro-inflammatory, and their levels correlated significantly with the severity of symptoms (Stanford University)

Interesting because many clinicians and researchers in this field have long believed that the disease was caused by abnormal cytokines in the brain.

- Synthesize molecules of inflammation (cytokines, prostaglandins) and elicit the production of those molecules by the gut immune system- Through inflammation, create a “leaky gut”: the tight junctions that bind gut epithelia cells together become loosened – allowing bacteria and bacterial toxins to enter the blood.

In addition to the recently-reported reduction in bacterial diversity in ME/CFS, the team reports finding an increased number of Caudovirales bacteriophage viruses in ME/CFS.

All of these findings point to low-level inflammation in the gut. (Cornell)

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Brain and Nervous System

- Impaired speed in processing information is shown to be a critical deficit in both ME/CFS and Gulf War Illness- Compared to healthy children, pediatric patients with ME/CFS had impaired information processing speed and attention. After exertion, these deficits worsened and ME/CFS kids also had poorer performance on tasks of working memory.- Impairments in cerebral blood flow and cortical glutathione levels – not affected by comorbid psychiatric disease.- A third of ME/CFS, but no healthy controls, had high white cell count or elevated protein in spinal fluid.- Altered heart rate variability, due to reduced cardiac vagal activity, in ME/CFS v. healthy controls. [There is some evidence that this can be a sign or contributory factor to heart disease later.]

Functional connectivity among different brain regions impaired:- Followed a cognitive test in ME/CFS v. healthy controls, determined by PET- As determined by diffusion MRI in GWI patients- As determined by EEG (eLORETTA) in ME/CFS patients at rest

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Epigenetic studies- Disease is caused not just by mutated genes- It also is caused by perfectly normal, non-mutated genes, when those genes are not “expressed” (turned on or off) appropriately- Gene expression is controlled by many different “epigenetic” forces- Epigenetic studies are increasingly being done in ME/CFS v. healthy control- ME/CFS: genes involved in signal transduction are hypomethylated more often, whereas genes involved in cell differentiation/cell death are hypermethylated more often- ME/CFS: significantly different gene expression patterns for genes, involved in immune regulation (JAK-STAT pathway), hormone regulation and mitochondrial dysfunction.- Gulf War Illness: 19 related groups of genes (“functional modules”) were found to have significantly altered gene expression. Specific immunosuppressant and hormonal therapies were identified that might target these dysregulated genes, and possibly improve symptoms.- ME/CFS patients, compared to healthy controls, have 13 different gene loci, all involving glucocorticoid sensitivity that are differentially methylated. The different methylation patterns correlated with clinical symptoms- Characteristic expression of two particular microRNAs in plasma leads to elevated homocysteine levels identified in ME/CFS- Three SNPs distinguished ME/CFS patients from healthy controls. All involve a gene that codes for a subunit of NADH dehydrogenase – an important energy molecule.- MicroRNAs in spinal fluid predict orthostatic tachycardia after exercise.- No clear gene expression differences in ME/CFS v. healthy controls, at rest.

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Energy Metabolism Studies- Studies on patients in the rituximab trial have an energy metabolism deficit, and the key molecule is the enzyme pyruvate dehydrogenase (PDH). Speculate that autoantiboedies may be the cause of this deficit. Upregulation of PDH inhibitors in white blood cells (Norway group – study will finish late 2017)- Peripheral white blood cells from ME/CFS produce energy less well than WBCs from healthy subjects, particularly when the cells are exposed to stressors.- Citric acid cycle metabolites are depleted. Glucose as an energy source is being replaced by fatty acids and amino acids- “Unbiased” metabolomics study finds that the metabolites that are most different between ME/CFS and healthy controls involve pathways harvesting energy from glucose, fatty acids and amino acids.- Also finds a general hypometabolic state, as did the recent paper from Naviaux (PNAS), though different metabolites were examined.

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Miscellaneous- ME/CFS patients, but not healthy controls, experience a worsening of symptoms following true (but not sham) strain: neuromuscular strain (even sitting/driving for prolonged time) may contribute to symptoms of ME/CFS. Physical therapy likely to help- Five specific findings on physical examination were quite accurate in diagnosing ME/CFS. This is of interest, since ME/CFS is defined exclusively by symptoms.- Of over 200 single-nucleotide polymorphisms examined, three – all located in the gene for NADH dehydrogenases – were significantly different in ME/CFS patients than in healthy controls.- ME/CFS patients have significantly higher anti-citrullinated protein antibodies than matched healthy controls, as is seen in the autoimmune whatever.- Particular mutations in two nucleosome transport genes distinguish ME/CFS patients from healthy controls.- A second case of ME/CFS caused by an enteroviral infection of the brain.- Impressive hypothesis: dysregulation in the production/release of Hydrogen Sulfide could explain many of the symptoms and objective abnormalities seen in ME/CFS- A subset of ME/CFS patients with sinusitis and/or hives has more pain and other symptoms

An ideal diagnostic test would:· Have very low false positive and false negative rates, compared to healthy controls and other fatiguing disease, when retested on a large number of new people· Be easy for perform reliably by many labs· Be inexpensive

Treatment Studies

· MRI spectroscopy revealed 15% lower levels of the natural antioxidant, glutathione, in the brain in ME/CFS patients compared to controls. N-acetyl-cysteine (NAC) treatment improved both brainglutathione levels and symptoms, and reduced oxidative stress, in the ME/CFS patients· Randomized trial of low-dose methylphenidate plus a nutritional regimen designed to improve mitochondrial function. At 12 weeks, a trend toward reduced symptom that was not statistically significant; more severely ill patients seemed to benefit· A careful study of 990 ME/CFS patients found that patient beliefs about the cause of their illness did not explain their level of activity, a result that does not support the theoretical benefit of cognitive behavioral therapy.· Multimodel physical therapy improves symptoms in adolescents and young adults with ME/CFS and impaired range of motion.· Quantitative modeling identifies drug that are already FDA-approved and that might target TNA-alpha, IL-2 and the glucocorticoid receptor – targets that may be important in causing the symptoms of GWI

Questions addressed by many presentations:· In an illness defined exclusively by subjective symptoms, is there evidence of underlying biological abnormalities?· Could those biological abnormalities theoretically explain the symptoms?· Do the abnormalities in fact correlate with the symptoms?

Author

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About me:I'm a 25-year veteran of CFIDS. I know what it is like to be bedbound for long stretches of time. I also know what it is like to recover, and to relapse. But this blog is not about my personal experience. It is intended to be a resource - a collection of anything that might be helpful to the CFIDS community: book reviews, advice, CFIDS news, research, advocacy, opinion, who's who in our community, fundraising... and occasionally a bit of humor.

Disclaimer: I am not a doctor, which means nothing I write, no matter how sensible it may be, should be interpreted as medical advice.